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PubMed1980

Reinnervation of the olfactory bulb after section of the olfactory nerve in monkey (Saimiri sciureus).

Section of the fila olfactoria in squirrel monkey, a non-human primate, induces rapid degeneration of the sensory axon terminals in the olfactory bulb glomeruli. A population of axons, from newly formed sensory neurons in the olfactory neuroepithelium, regrow, passes the lamina cribrosa and, upon reaching the olfactory bulb, reinnervates the glomeruli. A new set of synaptic contacts is reformed between the sensory terminals and the post-synaptic dendritic processes of the glomeruli. Our observations indicate that this portion of the CNS of a non-human primate can be reinnervated after deafferentiation, and that active synaptogenesis occurs.

Animals↗
PubMed1994

Morphological characteristics of cultured olfactory bulb cells.

Cultured olfactory bulb cells from embryonic mice had ultrastructural characteristics similar to those of many cell types in the intact adult mouse olfactory bulb. Identified cultured cells included mitral/tufted cells, granule cells, short-axon cells, and fibrous and protoplasmic astrocytes. Cultured neurons were found as individual cells, clusters or aggregates. Clusters consisted of a loose array of neurons that appeared to be densely interconnected by neurites. However, few neurites or fascicles emanated from clusters to adjoining areas. Aggregates consisted of many small, usually rounded, neurons piled on top of one larger neuron, or on more than one, with typically many neurites and fascicles projecting to adjacent aggregates, clusters or individual neurons. Neurites of cultured olfactory bulb cells were well developed, and some were several millimeters long. Synapses were very prominent in these cultures, especially in aggregates, clusters, and fascicles. Electron-lucent, dense-core, and coated vesicles were present. Polarity, shape, and length of the long axis (size) of 815 cultured neurons, identified by positive anti-microtubule-associated protein 2 staining, were documented. Cultured neurons varied in size from 9 to 27 microns, with an average size of 16 microns. Elliptical bipolar (35%), triangular multipolar (21%), and round unipolar (15%) were the most common polarity/shape combinations found in culture. Multipolar, triangular, triangular multipolar, and elliptical bipolar cells increased in size with increasing age of culture. The relative proportions of triangular, multipolar, elliptical multipolar, and triangular multipolar cells decreased, whereas the relative proportions of round, unipolar, and round unipolar cells increased with increasing age of culture. These changes in population subtypes and cell size may indicate continued differentiation and maturation of cultured neurons.

Animals↗
PubMed2002

Mapping at glomerular resolution: fMRI of rat olfactory bulb.

The rat olfactory bulb contains approximately 2000 functional units called glomeruli which are used to recognize specific characteristics of odorants. Activity localization of individual glomerulae ( approximately 0.002 microL) has important consequences for understanding mechanisms in olfactory information encoding. High-resolution functional MRI (fMRI) data from the rat olfactory bulb are presented using the blood oxygenation level dependent (BOLD) method at 7 T. Either individual or clusters of fMRI voxels suggestive of activity in the olfactory nerve and glomerular layers were reproducibly detected with repeated 2-min exposures of iso-amyl acetate at spatial resolution of 0.001-0.003 microL. The importance of glomerular clustering for olfaction and the implications of BOLD mapping with even higher spatial resolution (i.e., <<0.001 microL voxels) are discussed. High-resolution in vivo mapping of the rat olfactory bulb with fMRI at high magnetic field promises to provide novel data for understanding olfaction.

Animals↗
PubMed1992

The expression of the immediate-early genes c-fos, egr-1 and c-jun in the accessory olfactory bulb during the formation of an olfactory memory in mice.

Female mice form a memory for the pheromones of the male with which they mate. It has been proposed that the site of the synaptic changes underlying this memory is the accessory olfactory bulb, at the first level of the accessory olfactory system. In this study we have examined the expression of the immediate-early genes c-fos, c-jun and egr-1 in the mitral and granule cells of the accessory olfactory bulb immediately after mating, during the period of memory formation. Transient increases were seen in the number of granule cell nuclei expressing c-fos and the number of granule and mitral cell nuclei expressing egr-1, during the period of memory formation. No changes were observed in the expression of c-jun during this period. The increase in the number of cells expressing c-fos and egr-1 required the association of mating and pheromonal exposure, conditions also required for memory formation. Large increases in the number of mitral and granule cell nuclei expressing c-fos and egr-1 were also observed following the infusion of the drug bicuculline into the accessory olfactory bulb in the absence of mating. This procedure has previously been shown to result in the formation of a nonspecific memory for male pheromones. These results associate the expression of c-fos and egr-1 in the accessory olfactory bulb with the conditions required for the formation of an olfactory memory for male pheromones.

Animals↗
PubMed2006

Neuropeptide Y modulates excitatory synaptic transmission in the olfactory bulb.

Although the olfactory bulb contains one of the highest concentrations of neuropeptide Y in the CNS, its function in the bulb remains unclear. In this study, we used whole-cell electrophysiological, molecular, and primary culture techniques to investigate neuropeptide Y gene expression and neuromodulatory actions of neuropeptide Y on rat olfactory bulb neurons. Northern analysis showed that neuropeptide Y mRNA increases with animal age or time in culture, in a parallel manner. In electrophysiology experiments, agonists that activate neuropeptide Y receptors (whole neuropeptide Y) and the Y2 receptor subtype (neuropeptide Y 13-36) reduced spontaneous excitatory activity in bulb interneurons. In investigating potential presynaptic effects, both agonists reduced the amplitude of calcium channel currents in the presynaptic (mitral/tufted) cell. Also consistent with a presynaptic effect, both agonists reduced the frequency but not the amplitude of miniature excitatory postsynaptic currents (or "minis") in interneurons. In examining potential postsynaptic effects, both agonists slightly increased membrane resistance but had no effect on currents evoked by glutamate. Together, these data suggest that neuropeptide Y inhibits excitatory neurotransmission between olfactory bulb neurons via a presynaptic effect on transmitter (glutamate) release.

Animals↗
PubMed1994

Activation of opioid and muscarinic receptors stimulates basal adenylyl cyclase but inhibits Ca2+/calmodulin- and forskolin-stimulated enzyme activities in rat olfactory bulb.

In rat olfactory bulb, muscarinic and opioid receptor agonists stimulate basal adenylyl cyclase activity in a GTP-dependent and pertussis toxin-sensitive manner. However, in the present study, we show that in the same brain area activation of these receptors causes inhibition of adenylyl cyclase activity stimulated by Ca2+ and calmodulin (CaM) and by forskolin (FSK), two direct activators of the catalytic unit of the enzyme. The opioid and muscarinic inhibitions consist of a decrease of the maximal stimulation elicited by either CaM or FSK, without a change in the potency of these agents. [Leu5]-Enkephalin and selective delta- and mu-, but not kappa-, opioid receptor agonists inhibit the FSK stimulation of adenylyl cyclase activity with the same potencies displayed in stimulating basal enzyme activity. Similarly, the muscarinic inhibition of FSK-stimulated adenylyl cyclase activity shows agonist and antagonist sensitivities similar to those characterizing the muscarinic stimulation of basal enzyme activity. Fluoride stimulation of adenylyl cyclase is not affected by either carbachol or [Leu5]enkephalin. In vivo treatment of olfactory bulb with pertussis toxin prevents both opioid and muscarinic inhibition of Ca2+/CaM- and FSK-stimulated enzyme activities. These results indicate that in rat olfactory bulb delta- and mu-opioid receptors and muscarinic receptors, likely of the M4 subtype, can exert a dual effect on cyclic AMP formation by interacting with pertussis toxin-sensitive GTP-binding protein(s) and possibly by affecting different molecular forms of adenylyl cyclase.

Adenylyl Cyclases↗
PubMed1990

Ca2(+)-independent stimulation of adenylate cyclase activity by muscarinic receptors in rat olfactory bulb.

In rat olfactory bulb homogenate, carbachol stimulated adenylate cyclase activity in a concentration-dependent manner (EC50 = 1.1 microM). The carbachol stimulation occurred fully in membranes that had been prepared in the presence of 1 mM EGTA and incubated in a Ca2(+)-free enzyme reaction medium. Under these conditions, exogenous calmodulin (1 microM) failed to stimulate adenylate cyclase activity. In miniprisms of olfactory bulb, carbachol (1 mM) increased accumulation of inositol phosphates, but this response was markedly reduced in a Ca2(+)-free medium. Moreover, the carbachol stimulation of adenylate cyclase activity was not affected by staurosporine at a concentration (1 microM) that completely blocked the stimulatory effect of phorbol 12-myristate 13-acetate, an activator of Ca2+/phospholipid-dependent protein kinase. Quinacrine, a nonselective phospholipase A2 inhibitor, reduced the carbachol stimulation of adenylate cyclase activity, but this inhibition appeared to be competitive with a Ki of 0.2 microM. Nordihydroguaiaretic acid and indomethacin, two inhibitors of arachidonic acid metabolism, failed to affect the carbachol response. These results indicate that in rat olfactory bulb, muscarinic receptors stimulate adenylate cyclase activity through a mechanism that is independent of Ca2+ and phospholipid hydrolysis.

Adenylyl Cyclases↗
PubMed1997

Impairment of muscarinic stimulation of adenylyl cyclase by heparin in rat olfactory bulb.

In rat olfactory bulb membranes, the stimulation of adenylyl cyclase by the cholinergic agonist carbachol (CCh) was markedly inhibited by heparin at concentrations (0.3-10 microM) that had smaller or no effects on the enzyme stimulations elicited by vasoactive intestinal peptide, pituitary adenylate cyclase activating polypeptide (PACAP), 1-isoproterenol and corticotropin releasing hormone. Heparin did not significantly affect the binding of [3H]N-methylscopolamine ([3H]NMS) to muscarinic receptors, but decreased the potency of CCh in displacing the bound radioligand in a manner similar to that of the GTP analogue guanosine-5'-O-(3'-thio)triphosphate (GTPgammaS). Heparin inhibited the binding of [35S]GTPgammaS to membrane G proteins stimulated by CCh more potently than that elicited by PACAP. Moreover, at the same concentrations, heparin inhibited the muscarinic inhibition of adenylyl cyclase in rat striatal membranes. These data indicate that heparin impairs the muscarinic stimulation of olfactory bulb adenylyl cyclase likely by interfering with the receptor-induced activation of G proteins. The higher sensitivity to heparin of this response as compared to those displayed by Gs-mediated enzyme stimulations provides further evidence that Gi/Go, rather than Gs, mediate the muscarinic stimulation of adenylyl cyclase in rat olfactory bulb.

Adenylyl Cyclases↗
PubMed1995

Distribution of growth associated protein (B-50/GAP-43) and glial fibrillary acidic protein (GFAP) immunoreactivity in rat homotopic olfactory bulb transplants.

Recent studies on olfactory bulb homotopic transplantation after partial or subtotal bulb ablation have shown that regenerated olfactory axon are able to form glomeruli-like structures either in the transplant or in the spared olfactory bulb. To investigate the maturation of olfactory axons and their terminal connections in the transplant and remnant olfactory bulb we performed immunohistochemistry utilizing as markers B-50/GAP43 for neurite outgrowth and glial fibrillary acidic protein (GFAP) for the glial response to the surgery. Radioactively prelabeled olfactory bulbs (E 18) were homotopically transplanted in unilaterally bulbectomized neonatal rats (P6). Two to four months after transplantation in the partially bulbectomized rats the laminar organization of the olfactory bulb remnant depended on the extent of lesion. The transplant was disorganized showing irregularly distributed glomeruli. In a few cases pseudo-laminar organization was observed resembling that of the normal olfactory bulb. In 2 month-old transplants, outgrowing axons had a newly formed glomeruli displayed prominent B-50/GAP43 immunoreactivity. Four months after the operation B-50/GAP43 immunoreactivity was still present in the regrowing axons and some glomeruli in the transplant were B-50/GAP43 positive, while other glomeruli revealed a patchy pattern. The same B-50/GAP43 immunostained patchy structure were present in remnants of the lesioned olfactory bulb. Distinct increase of GFAP activity was observed along the olfactory axons and in the glomeruli-like structures. The persisting B-50/GAP43 immunoreactivity in the glomeruli of the transplant and in the remnants of lesioned olfactory bulb suggests that maturation of the newly formed glomeruli was delayed in comparison to the intact control olfactory bulb. Furthermore, the decrease of B-50/GAP43 immunoreactivity and the patchy distribution may indicate that synaptogenesis occurred in the glomeruli of the transplant, in spite of the altered topography. Together with previous findings on reinnervation of the piriform cortex from projection neurons situated in olfactory bulb transplants, our immunohistochemical data support the notion that olfactory bulb transplantation may reestablish to some degree the neuronal circuits affected by the experimental surgery.

Animals↗
PubMed1999

Multiple and opposing roles of cholinergic transmission in the main olfactory bulb.

The main olfactory bulb is a critical relay step between the olfactory epithelium and the olfactory cortex. A marked feature of the bulb is its massive innervation by cholinergic inputs from the basal forebrain. In this study, we addressed the functional interaction between cholinergic inputs and intrinsic bulbar circuitry. Determining the roles of acetylcholine (ACh) requires the characterization of cholinergic effects on both neural excitability and synaptic transmission. For this purpose, we used electrophysiological techniques to localize and characterize the diverse roles of ACh in mouse olfactory bulb slices. We found that cholinergic inputs have a surprising number of target receptor populations that are expressed on three different neuronal types in the bulb. Specifically, nicotinic acetylcholine receptors excite both the output neurons of the bulb, i.e., the mitral cells, as well as interneurons located in the periglomerular regions. These nicotine-induced responses in interneurons are short lasting, whereas responses in mitral cells are long lasting. In contrast, muscarinic receptors have an inhibitory effect on the firing rate of interneurons from a deeper layer, granule cells, while at the same time they increase the degree of activity-independent transmitter release from these cells onto mitral cells. Cholinergic signaling thus was found to have multiple and opposing roles in the olfactory bulb. These dual cholinergic effects on mitral cells and interneurons may be important in modulating olfactory bulb output to central structures required for driven behaviors and may be relevant to understanding mechanisms underlying the perturbations of cholinergic inputs to cortex that occur in Alzheimer's disease.

2-Amino-5-phosphonovalerate↗
PubMed1994

Recovery of olfactory behavior. I. Recovery after a complete olfactory bulb lesion correlates with patterns of olfactory nerve penetration.

The olfactory system is an excellent system in which to study issues related to potential functional recovery after a debilitating brain injury. The olfactory system is well-characterized, easily accessible and there are a vast number of studies available from a variety of perspectives. The experimental aim of this research is to examine the anatomical correlates associated with potential behavioral recovery in rats that receive complete olfactory bulb lesions as neonates or as adults. The results show that behavioral recovery occurs only when olfactory nerve penetration of the central nervous system is observed. Further, both olfactory nerve penetration and behavioral recovery are age-dependent phenomena. The olfactory nerve penetration only occurs when the olfactory bulb lesion is performed in neonates. Behavioral recovery of olfactory ability follows a linear trend and reaches near normal levels during the six weeks behavioral testing period. Histological analysis using an antibody for olfactory marker protein (an olfactory nerve-specific marker) reveals two potential candidates for the anatomical pathway responsible for behavioral recovery: olfactory nerve to orbital frontal cortex and olfactory nerve to olfactory peduncle. This report presents evidence that recovery of olfactory ability can occur in the absence of the olfactory bulb if the lesion is performed when the rat is still a neonate.

Animals↗
PubMed2000

Acetylcholine induces neuritic outgrowth in rat primary olfactory bulb cultures.

The rat olfactory bulb is innervated by basal forebrain cholinergic neurons and is endowed with both nicotinic and muscarinic receptors. The development of this centrifugal cholinergic innervation occurs mainly in early postnatal stages. This developmental time-course and the demonstration that acetylcholine can modulate some aspects of neuronal proliferation, differentiation or death, suggests the possible involvement of cholinergic afferents in the morphogenesis and/or plasticity of the olfactory bulb. The purpose of the present work was to assess whether acetylcholine could modulate neuronal morphogenesis in the olfactory bulb. Toward this aim, we developed a primary culture model of rat olfactory bulbs. Three major cell types were identified on the basis of their morphological and immunocytochemical phenotype: neuronal-shaped cells expressing the neuronal markers neuron specific enolase, microtubule associated protein 2, neural cell adhesion molecule and beta-tubulin III; glial-like cells immunoreactive for glial fibrillary acidic protein and flattened cells immunolabelled with antibodies against beta-tubulin III and nestin, most likely neuronal precursors. After three to six days of treatment with 100-microM carbachol, a cholinergic agonist, significant increase in neuritic length was observed in cultured olfactory bulb neurons. The neurite outgrowth effect of carbachol was abolished by co-treatment with 1 microM alpha-bungarotoxin, an alpha 7 subunit nicotinic receptor antagonist, but was not affected by the addition of 10 microM atropine, a general muscarinic antagonist. The effect of carbachol was also mimicked by the nicotinic agonists, nicotine (100 microM) and epibatidine (10 microM). This pharmacological profile suggested the involvement of nicotinic receptors of the alpha 7-like subtype as confirmed using 125I-alpha-bungarotoxin receptor autoradiography.Taken together, these data argue for a role for nicotinic receptors in neuritic outgrowth in the rat olfactory bulb and provide a cellular support to the previously described effects of acetylcholine on olfactory bulb plasticity in vivo.

Acetylcholine↗
PubMed1999

Ribosomal RNA expression in the developing rat olfactory bulb.

The rat olfactory bulb undergoes rapid postnatal growth, thus requiring the continuous production of new proteins. The present study examined the development of ribosomes, a key component in protein synthesis, in the bulb using an antibody specific to ribosomal RNA (Y10b). Furthermore, the potential role of afferent activity on patterns of Y10b immunoreactivity, as well as total RNA production (using incorporation of 3H-uridine) was examined by blocking an external naris on postnatal day 1 (P1). In control pups, Y10b was restricted to mitral cells at P2, with labeling expanding to include all layers by P10. Considerable increases in staining density were observed by P30. Although no differences in Y10b immunoreactive patterns were seen in naris-occluded animals 12-48 h after occlusion, or on P10 or P20, by P30, an apparent decrease in numbers of labeled profiles (presumably tufted cells) in the external plexiform layer was found. Furthermore, no changes were seen in levels of 3H-uridine incorporation. Despite the apparent insensitivity to naris closure, the results indicate that ribosome expression, as measured by Y10b immunoreactivity, undergoes rapid postnatal changes that parallel general patterns of growth in the rat olfactory bulb.

Animals↗
PubMedDate not supplied

[Protocortex versus protomap: a perspective from the olfactory bulb].

INTRODUCTION AND AIM: The olfactory sensory system is a unique model for the research of guidance and connectivity of growing axons. During development, the olfactory epithelium, the olfactory bulb and the olfactory cortex differentiate several cell types and extend projection axons. Because there is a close relationship between these three structures, we ask the question as to whether establishment of the olfactory bulb central projections can proceed independently of the arrival of the olfactory sensory afferents. This raises another more general question: is establishment of afferent connections necessary to awake a developmental program in target cells?. DEVELOPMENT: The initial establishment of the olfactory bulb central projections occurs independently of the arrival of the olfactory axons from the olfactory epithelium, which reinforces the idea that cortical regions are already patterned before migration of newborn neurons, at least for the olfactory bulb and maybe for the entire brain. This implies a strict intrinsic molecular control of the distinct olfactory structures, independent one of each other. CONCLUSIONS: How then, do axonal projections find their correct way within the brain? Contact-mediated mechanisms and chemotropic molecules cooperate to fix their position in the telencephalon, prevent bulbar axons from invading structures other than the olfactory cortex and, at the same time, stimulate axonal branching in an orchestra of both, attractive/promoting and repulsive/inhibiting signals. At later stages, the mature appearance of the olfactory bulb will be completed and refined.

Animals↗
PubMed1994

Information coding in the olfactory system: evidence for a stereotyped and highly organized epitope map in the olfactory bulb.

In the mammalian olfactory system, information from approximately 1000 different odorant receptor types is organized in the nose into four spatial zones. Each zone is a mosaic of randomly distributed neurons expressing different receptor types. In these studies, we have obtained evidence that information highly distributed in the nose is transformed in the olfactory bulb of the brain into a highly organized spatial map. We find that specific odorant receptor gene probes hybridize in situ to small, and distinct, subsets of olfactory bulb glomeruli. The spatial and numerical characteristics of the patterns of hybridization that we observe with different receptor probes indicate that, in the olfactory bulb, olfactory information undergoes a remarkable organization into a fine, and perhaps stereotyped, spatial map. In our view, this map is in essence an epitope map, whose approximately 1000 distinct components are used in a multitude of different combinations to discriminate a vast array of different odors.

Animals↗
PubMed1993

The quantitative relationship between olfactory axons and mitral/tufted cells in developing Xenopus with partially deafferented olfactory bulbs.

Partial deafferentation of the olfactory bulb in Xenopus embryos was performed to analyze the effects of afferent innervation on the development of the central olfactory structure. In an attempt to analyze a possible early inductive role of the olfactory axons, one olfactory placode was removed before differentiation of the neural tube began (stages 26-31). A morphological and quantitative analysis was performed on larvae at the onset of metamorphic climax (stage 58). When the single olfactory nerve innervated one side of the rostral telencephalon, a single olfactory bulb developed on that side and no olfactory bulb formed on the contralateral side. When the nerve innervated the midline of the rostral telencephalon, a smaller-than-normal, fused olfactory bulb developed. Partial deafferentation at these early stages resulted in a significant reduction in the number of olfactory axons (to approximately one-half of control values) and a corresponding decrease in the number of mitral/tufted cells (output neurons of the olfactory bulb). To control for possible damage to the neural tube during olfactory-placode removal, a portion of the neural tube directly beneath one of the olfactory placodes was removed in embryos. In these animals, the neural tube regenerated within 24 h and formed a normal olfactory bulb; olfactory axon and mitral/tufted-cell numbers were not significantly different from controls. In conclusion, olfactory-afferent innervation was critical for differentiation of the olfactory bulb, and decreasing the number of olfactory axons resulted in a reduction in the number of output neurons of the olfactory bulb.

Animals↗
PubMed1990

Early unilateral deprivation modifies olfactory bulb function.

Unilateral olfactory deprivation during postnatal development produces significant structural and neurochemical modifications of the olfactory bulb. In the present report, we describe the functional consequences of such deprivation. Rat pups had a single naris occluded on postnatal day 2 (PN2) to deprive them of early olfactory stimulation. On PN20-22, the occluded naris was reopened, the previously open naris was sealed, and responses of the deprived olfactory bulb to odors were assessed using both single-unit recording from mitral/tufted cells and quantitative 14C-2-deoxyglucose (2-DG) autoradiography. While the response properties of individual odor-stimulated mitral/tufted cells were not altered by early deprivation, spontaneous activity was depressed, and there was a significantly higher incidence of odor-responsive mitral/tufted cells in deprived compared to nondeprived bulbs. In addition, odor-stimulated deprived bulbs demonstrated greater uptake of 2-DG than did non-deprived bulbs. Together, these data indicate that the olfactory system demonstrates an increased responsiveness to sensory cues following early deprivation.

Animals↗